This paper describes analytical and simulation models of the population dynamics of transposable elements in randomly mating populations. The models assume a finite number of chromosomal sites that are occupable by members of a given family of elements. Element frequencies can change as a result of replicative transposition, loss of elements from occupied sites, selection on copy number per individual, and genetic drift. It is shown that, in an infinite population, an equilibrium can be set up such that not all sites in all individuals are occupied, allowing variation between individuals in both copy number and identity of occupied sites, as has been observed for several element families in Drosophila melanogaster. Such an equilibrium requires either regulation of transposition rate in response to copy number per genome, a sufficiently strongly downwardly curved dependence of individual fitness on copy number, or both. The probability distributions of element frequencies, generated by the effects of finite population size, are derived on the assumption of independence between different loci, and compared with simulation results. Despite some discrepancies due to violation of the independence assumption, the general pattern seen in the simulations agrees quite well with theory.

Data from Drosophila population studies are compared with the theoretical models, and methods of estimating the relevant parameters are discussed.

A new mutant (Wct) has been identified at the W locus of the mouse. The homozygote is poorly viable. Whereas the heterozygote (Wct / +) is only mildly anaemic like Wυ / +, the double heterozygote Wct + / + Ph is considerably more anaemic than Wυ + / + Ph and it and Wsh + / + Ph have significantly raised leucocyte counts. Wct + / + Ph is also unduly radiosensitive to whole body X-irradiation, 50% dying from haematopoietic failure at a dose of 4·59 ± 0·14 Gy, whereas the median for Wct / + was 6·49 ± 0·28 Gy. Serial blood counts of mice after low- or sub-lethal doses of X-rays revealed significantly more profound depression of counts of both red cells and leucocytes in Wct +, and more notably in Wct + / + Ph, than in + / + or Wsh / + (haematologically normal) iso-dosed mice. We conclude that control of haematopoiesis by chromosome 5 is not confined to the W locus but is shared by the linked gene Ph (and perhaps Rw) and that expression of the change is not limited to the erythron but involves the pluripotent haematopoietic stem cell.

Amoebae and plasmodia are alternate vegetative forms in the life cycle of the acellular slime mould Physarum polycephalum. Haploid amoebae carrying heterothallic alleles of the matA (or mt) locus ordinarily form plasmodia only by crossing, but occasionally give rise to mutants that form plasmodia by selfing as well as by crossing. Twelve independently isolated mutants of this type have been studied. Eight carry mutations (termed gad or greater asexual differentiation mutations) within approximately 0·2 map units of matA. Another mutation (gad-12) is linked neither to matA nor to any of 9 other markers tested. The remaining three mutations are linked to matA and map as follows: matA–0·5 units – gad-4–4 units – gad-6 – 8 units – gad-11. One mutation, gad-11, has been tested in strains carrying each of the five matA alleles (matAl, 2, 3, 4, and h) available in a common genetic background; the mutation is expressed with all five alleles. The mutation npfF1 (formerly aptA1), which was isolated as a suppressor of selfing in Colonia (matAh) amoebae, suppresses the action of each of the 12 gad mutations. The similarly isolated mutation npfA1 is also epistatic to eight of the mutations, but permits selfing with gad-5, 6, 12 and 13. For double mutant strains containing gad-12 and gad-1, 2, 4, 6 or 11, the selfing behaviour of each double mutant differs from that of either single mutant. Mixtures of gad−npfF1 with gad+npf+ amoebae readily form plasmodia, a result suggesting that gad mutations are dominant or semi-dominant. We conclude that the commitment of a cell to differentiate into a plasmodium is under the control of a complex group of genes linked to matA.

Using seven newly induced duplications, three Minute loci have been located cytologically: M(3)hS 37 in 65F10–11; 66A (a new Minute locus), M(3)i in 67C, and M(3)hy in 68F; 69F. M(3)hS 37 and M(3)hy were previously thought to be allelic because they do not complement for lethality. The finding of Minute mutations with additive or synergistic rather than epistatic interactions makes us suspect that some other Minute mutations have been erroneously called allelic. The involvement of Minute loci in more than one biochemical pathway is discussed in view of the existence of synergistic interactions and of Minute loci without known mutant alleles.

We report the results of an ontogenetic analysis of quantitative genetic variance components with two replicates drawn from the randombred ICR strain of mice. A total of 432 mice from 108 full-sib families raised in a cross-fostering design were used to estimate direct effects heritability, maternal effects, and environmental effects for weight, head length, trunk length, trunk circumference, and tail length at 17, 24, 31, 38, 45, 52, 59, and 66 days of age. There was no significant difference in heritability between the replicates. Heritabilities either stayed more or less constant with age at about 0·30 (weight, trunk length, trunk circumference) or increased slightly with age (head length, tail length). Maternal effects decreased with age from a maximum of about 0·50 at weaning to about 0·15 at age 66 when growth was nearly complete. Environmental effects increased in relative importance during ontogeny.

The expression of electrophoretic variant forms of the X-linked enzyme phosphoglycerate kinase (PGK-1) was examined during the ontogeny of the female germ-line following X-chromosome reactivation. Non-growing oocytes from foetal and neonatal ovaries of heterozygous females show a higher PGK-1A isozyme activity, a reflection of prior non-random X-inactivation favouring activity of the X-chromosome carrying the Pgk-1a allele and Xcec locus. On oocyte growth, the total PGK-1 enzyme activity increases 40–50 fold and the pattern of PGK-1 isozyme expression changes giving an electrophoretic pattern now skewed in favour of the PGK-1B isozymic form. Activity of the PGK-1B isozyme exceeds that of PGK-1A in all growing oocytes with a total activity greater than 0·075 nmol h−1 oocyte−1. Mice homozygous for either Pgk-1 allele show similar PGK-1 specific activities in somatic tissues where one X-chromosome is active, but oocytes of Pgk-lb homozygotes show a higher specific activity compared to those of Pgk-1a homozygotes. Thus increased activity of the PGK-1B isozyme relative to the PGK-1A isozyme is specific to growing oocytes.

Heterokaryons of N. crassa were synthesized from homokaryotic strains differing in sterol composition and sensitivity to the polyene antibiotic nystatin. Mycelia of the nystatin-sensitive strain erg-1+ contained ergosterol and episterol, and the nystatin-resistant mutant erg-1 contained fecosterol and lichesterol. Mycelia of heterokaryons with different proportions of erg-1+: erg-1 nuclei contained various proportions of the four sterols. Ergosterol was the principal sterol in heterokaryons with more than 5% erg-1+ nuclei.

Heterokaryons with various proportions of erg-1+:erg-1 nuclei were grown for several weeks along tubes of synthetic media. Growth rates were stable on minimal medium and nutritionally supplemented media but nuclear proportions often fluctuated. Growth rates fell sharply on nystatin-supplemented media and there were adaptive increases in proportions of mutant erg-1 nuclei which resulted in selection of nystatin-resistant homokaryotic mycelia.

The effect of the P-M system of hybrid dysgenesis in Drosophila melanogaster on unequal crossing-over was studied using the Bar duplication. This system of dysgenesis had no demonstrable effect on the rate of Bar reversion. In the course of the study it was found that there was a greatly reduced rate of reversion in two homozygous inversion stocks. Further, one revertant was found which may result from unequal crossing over at the Bar locus in males.